RACP Divisional Written Exam · FRACP

Rheumatology/Immunology for the written exam

Everything Physify has for Rheumatology/Immunology: short lessons written to Australian guidance, exam-style questions with a worked explanation for each, and Bedside, our AI tutor, under every one. Try a question below, no sign-up.

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37courses
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130lessons
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947exam-style questions
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29figures in the lessons

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Rheumatology/Immunology

A 63 year old woman in Adelaide had a negative iFOBT through the National Bowel Cancer Screening Program 12 months ago. She has no symptoms, no family history of colorectal cancer and a normal haemoglobin. A friend does a stool test every year, and she asks whether she should do another kit now. What is the most appropriate advice?

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What's covered

37 courses, each a set of lessons with a quiz after them. The bar shows how many questions each has. Open a course to see its lesson outline.

From the lessons

29 figures sit in the Rheumatology/Immunology lessons: ECGs, diagrams, films and clinical images, each with what to look for. Here are 4. Tap one to enlarge it.

Schematic of the 2012 Chapel Hill nomenclature laid along the vessels, drawn as cross-sections from the aorta through large, medium (visceral), small arteries and arterioles to capillaries, venules and veins. Large vessel vasculitis (giant cell arteritis, Takayasu arteritis) predominantly affects the aorta and large arteries: limb claudication, absent pulses and stroke, with headache, jaw claudication and visual loss in giant cell arteritis. Medium vessel vasculitis (polyarteritis nodosa, Kawasaki disease) predominantly affects medium arteries: aneurysms, infarcts and mononeuritis; polyarteritis nodosa spares arterioles, capillaries and venules, so there is no glomerulonephritis. ANCA associated, pauci-immune small vessel vasculitis affects small arteries to venules: granulomatosis with polyangiitis (PR3, cytoplasmic), microscopic polyangiitis (MPO, perinuclear) and eosinophilic granulomatosis with polyangiitis (MPO, perinuclear, when ANCA positive), with glomerulonephritis, alveolar haemorrhage and palpable purpura. Immune complex small vessel vasculitis (anti-GBM disease with linear IgG, cryoglobulinaemic vasculitis, IgA vasculitis, hypocomplementaemic urticarial vasculitis with anti-C1q) mainly affects capillaries and venules, sometimes arterioles, and rarely arteries. Variable vessel vasculitis (Behcet disease, Cogan syndrome) affects arteries and veins of any size, with venous thrombosis and pulmonary artery aneurysm in Behcet disease. Dashed extensions show that any size artery can be involved in the three major categories. Notes list the other categories (single-organ vasculitis such as isolated aortitis and primary CNS vasculitis; vasculitis with lupus, rheumatoid disease or sarcoid; and vasculitis with a probable cause, such as hepatitis B and C, syphilitic aortitis, drugs and cancer) and the mimics to exclude before immunosuppressing: endocarditis, cholesterol emboli, atrial myxoma, antiphospholipid syndrome and levamisole-adulterated cocaine.
Physify teaching diagram (schematic), using the 2012 revised Chapel Hill nomenclature. Tap the image to zoom.

From the lesson “ANCA Testing & The Clinical Syndromes” in Small-Vessel Vasculitides

Schematic of the natural history of HIV infection on a broken time axis, weeks then years, in two panels. Top, CD4 count: a transient fall during acute infection, a partial recovery, then a slow decline over years of clinical latency until it crosses 200 cells per microlitre, where AIDS begins. Bottom, viral load on a log scale: a very high peak during acute infection, when the person is most infectious, falling to a set point that predicts the pace of progression, then rising again as AIDS develops. A bracket marks the seroconversion illness 2 to 4 weeks after exposure, with fever, sore throat, rash and lymphadenopathy. A green line marks diagnosis and the start of antiretroviral therapy, at any CD4 count; with treatment the viral load falls below the limit of detection, and undetectable means untransmittable, while the CD4 count recovers. AIDS is a CD4 count under 200 or an AIDS-defining illness at any count.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Testing, Staging & Antiretroviral Therapy” in Human Immunodeficiency Virus (HIV) & AIDS

The four Gell and Coombs hypersensitivity types, each with a small picture of its mechanism. Type I, immediate: allergen cross-links specific IgE on a mast cell, which releases histamine, tryptase, leukotrienes and prostaglandins within minutes (rarely up to 2 hours, with a late phase at 4 to 8 hours); examples anaphylaxis, allergic rhinitis and asthma, acute urticaria, food and venom allergy; tested by skin prick or specific IgE, and serum tryptase after a reaction. Type II: IgG or IgM binds antigen fixed on a cell or matrix, causing complement lysis, phagocytosis or a change in receptor function over hours to days; examples autoimmune haemolytic anaemia, immune thrombocytopenia, anti-GBM disease, myasthenia gravis (blocking) and Graves disease (stimulating); tested by the direct antiglobulin test and linear immunofluorescence. Type III: soluble immune complexes deposit in vessels, glomeruli and joints and activate complement and neutrophils; serum sickness at 7 to 14 days after first exposure and the Arthus reaction at 4 to 12 hours; examples serum sickness, lupus nephritis and post-streptococcal glomerulonephritis; low C3 and C4 and granular immunofluorescence. Type IV, delayed: sensitised T cells release cytokines or kill directly, recruiting macrophages and eosinophils, at 48 to 72 hours for contact and tuberculin reactions and days to weeks for severe drug reactions; examples allergic contact dermatitis, the tuberculin reaction, DRESS, Stevens-Johnson syndrome and toxic epidermal necrolysis; tested by patch testing and skin biopsy. Types I to III are antibody mediated and type IV needs no antibody.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Tolerance, Autoimmunity, Immune Checkpoints and Hypersensitivity” in Principles of Immunology

Schematic of a right hand seen from the back, labelled with the distal interphalangeal (DIP), proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints, the first carpometacarpal (CMC) joint at the thumb base and the wrist, then four hands with the typically involved joints shaded and typically spared joints dashed. Rheumatoid arthritis: symmetrical, MCPs, PIPs, thumb MCP and wrist shaded, DIPs spared. Osteoarthritis: DIPs (Heberden nodes), PIPs (Bouchard nodes), the thumb interphalangeal joint and the first CMC shaded; MCPs and wrist spared. Psoriatic arthritis: DIP-predominant and asymmetric, with a whole swollen sausage digit (dactylitis) and nail pitting. Gout: any joint, asymmetric, here a PIP and the wrist, with tophi beside the finger joints; the classic site is the first metatarsophalangeal joint. Patterns overlap, and gout and psoriatic arthritis can mimic rheumatoid arthritis.
Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Articular Patterns & The Acute Monoarthritis” in Approach to the Patient with Joint Pain

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Rheumatology/Immunology in the clinical exam

14 interactive short cases and 5 long cases for the RACP Divisional Clinical Exam: you examine, present and are marked on the five RACP domains.

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Rheumatology/Immunology on the blog

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